PTH - the connection of all stress hormones

Mauritio

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"When there is adequate calcium, vitamin D, and magnesium in the diet, PTH is kept to a minimum. When PTH is kept low, cells increase their formation of the uncoupling proteins, that cause mitochondria to use energy at a higher rate, and this is associated with decreased activity of the fatty acid synthase enzymes."
-Ray Peat


In the recent podcast with Ray he talks a about PTH beeing at the root of the whole stress cascade and vice versa stress hormones increasing PTH .
Danny roddy shared some studies in the comment ,that I thought more people would appreciate.

So lowering stress hormones should indirectly lower PTH.
Let's compile some more studies and things that lower PTH:

Directly lowering PTH:
• Calcium
• Magnesium
• Vitamin D
• Vitamin K
• Caffeine
• Famotidine



Here is some evidence for estrogen, prolactin , serotonin ,cortisol and aldosterone stimulating PTH and vice versa:


Society for Women's Health Research. Nutrition research: the unique needs of women. 2000. “It is well known, for example, that estradiol (the major estrogen secreted by the ovaries) increases the expression of parathyroid hormone (PTH) and calcitonin, the principle hormones involved in calcium regulation.”

Raymond, J., et al. Comparison between the plasma concentrations of prolactin and parathyroid hormone in normal subjects and in patients with hyperparathyroidism or hyperprolactinemia. J Clin Endocrinol Metab. 1982 Dec;55(6):1222-5. "These results show that an excess of plasma prolactin is associated with an excess of plasma PTH and vice versa."

Zimmerman, D., et al. Serotonin stimulates adenosine 3',5'-monophosphate accumulation in parathyroid adenoma. J Clin Endocrinol Metab. 1980 Dec;51(6):1274-8. "The present observations demonstrate that parathyroid adenoma tissue has a high content of serotonin, and serotonin stimulates cAMP accumulation in this tissue. Since cAMP acts as a mediator of parathyroid hormone (PTH) release, our results suggest that serotonin could be one of the factors regulating PTH secretion and/or contributing to PTH hypersecretion in various forms of primary hyperparathyroidism."


Constance R. Martin. Endocrin Physiology. 1985 "Glucocorticoids acutely elevate plasma calcium, probably because they stimulate parathyroid hormone secretion..."

Vaidya A, Brown JM, Williams JS. The renin-angiotensin-aldosterone system and calcium-regulatory hormones. J Hum Hypertens. 2015;29(9):515-521. "Growing evidence points to a bi-directional and positive relationship between the Renin-Angiotensin-Aldosterone System and PTH."
 

gaze

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while I partially agree in theory, i dont think its the entire picture. at a time when my calcium was slightly above range, my PTH was below the lower range of "normal" (because blood calcium decreases PTH), but during that time I was under extreme stress and anxiety. When I brought my blood calcium down to the middle of the range, my PTH rose a little to in the range but still low, and I felt much better. So just decreasing PTH at all costs will not solve all problems, because overly high blood calcium, which is not good, can also decrease PTH
 
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Mauritio

Mauritio

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This Textbook was recommended by ray as a generell overview of endocrinology. There's a lot more but I cant copy it all. I'll upload the book.


TEXTBOOK OF ENDOCRINE PHYSIOLOGY
Constance R. Martin, Ph.D.


REGULATI ON OF PARATHYROID
HORMONE SECRETION
By sharp contrast, very different mechanisms are required for regulation of parathyroid gland function. The parathyroid hormone acts rapidly on kidney and more slowly on bone to elevate calcium ion concentrations of the blood plasma . A very brief period of calcium ion deficiency leads to heightened neuromuscular excitabil ity
which is manifested first in exaggerated reflex responses, but is soon fol lowed in rapid succession by involuntary tremors, muscle spasms, convulsions, and finally release
to renal excret ion of inorganic
Phosphate is increased, with the result that
some of the plasma calcium previously
associated with phosphate becomes available as free calcium ion, as renal loss of calcium may be promptly diminished .
Parathyroid hormone also acts more slowly to
Release calcium from bone reserves, and continued calcium deficiency stimulates parathyroid hormone synthesis . High levels of calcium ion in the circulating blood exert an inhibitory influence on cells of the parathyroid gland.The control mechanism is summarized m Ftgure 2-4. A second hormone, calcitonin (CT, thyrocalcitonin), produced in the thyroid
glands of mammals by cells not involved in
thyroxine secretion ( and in the ultimo-
branchial bodies of other vertebrates) , has
been implicated in protection against an
excessive rise in the calcium ion concentra-
tion of the blood plasma. Its secretion is
triggered by the calcium rise. CT may be
needed under special circumstances (e.g. ,
during absorption of a calcium-rich meal
following a period of fasting) because the
inhibitory influence of calcium ions on the
secretion of parathyroid hormone may not
exert sufficiently rapid influences on blood
concentrations of the ion. CT favors reten-
tion of calcium and phosphate in bone, an
influence which is effectively ( but not directly) antagonistic to the actions of para-
thyroid hormone.
Additional details on regulation of calcium ion concentrations not directly relevant to this discussion are presented in
Section IV.


Parathyroid hormone influences on renal
phosphate and calcium excretion have been
widely studied. But the hormone also promotes
excret ion of sodium, potassium, bicarbonate,
and water, and high doses can induce dehydra-
t ion. Parathyroid hormone also decreases excre-
tion of magnesium and ammonium ions. High
plasma calcium levels which follow administra-
tion of the hormone have been i mplicated in
i nhibition of ADH actions on the renal distal
tubule and collecting ducts.

Lactate Formation and Related Con-
cepts. Other investigators called attention
to the increased rate of glycolysis in bone
after administration of parathyroid hor-
mone, and suggested that lactate ( rather
than citrate) is the agent responsible for
bone decalcification. A further modifica-
tion of the general concept states that it is
the reduction of pH in bone tissue (rather
than the accumulation of a specific anion)
which promotes bone solubilization. Car-
bonic acid has also been proposed to con-
tribute to acidity changes.
 

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Mauritio

Mauritio

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Policosanol lowers PTH . Rats that were put on an atherogenic diet, had a 3 times higher PTH than the controll group ,which the policosanol was able to reverse !


Also policosanol lowers aldosterone about 45% ,which is another mechanism of lowering PTH .

Post in thread 'The Policosanols Thread' The Policosanols Thread
 

Inaut

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I was making notes about PTH after listening to podcast. So happy you posted the above. Thanks @Mauritio

:) :) :)
 

tankasnowgod

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So lowering stress hormones should indirectly lower PTH.
Let's compile some more studies and things that lower PTH:

Directly lowering PTH:
• Calcium
• Magnesium
• Vitamin D
• Vitamin K
• Caffeine
• Famotidine

I think Calcium might be the most important. Consider this study-


A low calcium diet raised estrogen and PTH. Rats treated with K2 (and also elcatonin) on the low calcium diet were able to maintain bone density..... but PTH was even higher than just the rats on a low calcium diet-

Estrone Rats.png


PTH Rats.png


It somewhat makes sense. That calcium would have to come from somewhere, so with K2 keeping it in the bones, PTH and activated Vitamin D might have also helped to absorb more from the intestine, and prevent the excretion in the urine.

Still, I'm sure the rats would have been better off with adequate calcium and K2.
 
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Mauritio

Mauritio

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I think Calcium might be the most important. Consider this study-


A low calcium diet raised estrogen and PTH. Rats treated with K2 (and also elcatonin) on the low calcium diet were able to maintain bone density..... but PTH was even higher than just the rats on a low calcium diet-

View attachment 27236

View attachment 27237

It somewhat makes sense. That calcium would have to come from somewhere, so with K2 keeping it in the bones, PTH and activated Vitamin D might have also helped to absorb more from the intestine, and prevent the excretion in the urine.

Still, I'm sure the rats would have been better off with adequate calcium and K2.
Yes , i follow your logic. I think calcium, vitamin D and magnesium are the most potent. At least that's what ray mostly recommends for conditions with a high PTH .

There's also this study showing :"Vitamin K supplementation stimulates renal calcium reabsorption, increases maturation-related cancellous bone gain, and retards the reduction in maturation-related cortical bone gain, whereas vitamin D supplementation stimulates intestinal calcium absorption and prevents the reduction in maturation-related periosteal bone gain by inducing accumulation of calcium from cancellous and endocortical bone."

So in this case a low calcium + vitamin d/k or d+k did NOT lead to an elevation in PTH. Maybe it was the dosage ( 30mg Vitamin K/100g food) ...
Also the D+K combo was not more effective.
I'd like to know which vitamin was more effective at lowering PTH but cant find the full study on scihub .

 
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Mauritio

Mauritio

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I was making notes about PTH after listening to podcast. So happy you posted the above. Thanks @Mauritio

:) :) :)
No problem . I think it cant be overstated how important it is to keep PTH low .
 
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Mauritio

Mauritio

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I think Calcium might be the most important. Consider this study-


A low calcium diet raised estrogen and PTH. Rats treated with K2 (and also elcatonin) on the low calcium diet were able to maintain bone density..... but PTH was even higher than just the rats on a low calcium diet-

View attachment 27236

View attachment 27237

It somewhat makes sense. That calcium would have to come from somewhere, so with K2 keeping it in the bones, PTH and activated Vitamin D might have also helped to absorb more from the intestine, and prevent the excretion in the urine.

Still, I'm sure the rats would have been better off with adequate calcium and K2.
I changed my proxy to USA now it worked, I think scihub doesnt work for germany anymore.

So actually vitamin D solo was a lot more effective at lowering PTH than vitamin K .
Low calcium diet PTH: 1087
Low calcium + K : 651
Low calcium + D : 158
Normal calcium control group: 128

Screenshot_20210829-222326_Drive.jpg
 
Last edited:
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Mauritio

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This study shows that 24 months of estrogen treatment in old japanese people doubled there PTH .
The bone mineral density didn't change.

"In Group 3, serum level of parathyroid hormone (PTH) was significantly (p less than 0.05) increased from 0.28 +/- 0.03 ng/ml before the treatment to 0.55 +/- 0.15 ng/ml at 24 months after the treatment."

There was a very interesting group (4) which received amongst others : pregnenolone, testosterone and thyroid and after 24 months their bone mineral density increased 12%!

"Group 4 (n = 13, mean age; 76.4 +/- 1.8 y.o.) was treated with sex-steroids (pregnenolone : androstenedione : androstenediol : testosterone : estrone = 1.0 mg : 1.0 mg : 0.5 mg : 0.1 mg : 5 micrograms/tablet) and thyroid hormone (thyroid-sicca 7.5 mg/tablet) preparation in a dose of 2 tablets/day"


 
Last edited:
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Mauritio

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PaRa

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crazy that

adrenaline raises PTH

PTH raises histamine

While knowing that histamine lowers adrenaline
 
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Mauritio

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Mauritio

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Here are some more good studies from Danny Roddys telegram :

2.…It is important to point out that low levels of parathyroid hormone (PTH) are essential for maintaining healthy bone structure and normal remodeling."
— Endocrine Physiology by Constance R. Martin

3. PTH and 1,25-D (calctriol or "active" vitamin D) cause hypercalcemia and calcification:

"Severe hypercalcemia is mainly caused by inappropriately high concentrations of compounds which promote bone resorption, in particular PTH, PTHrP, or 1,25-D."



4. The popular "metabolic syndrome,” that involves diabetes, hypertension, and obesity, is associated with higher parathyroid hormone (PTH):

"The PTH level... is an independent predictor of metabolic syndrome..."


5. PTH tends to rise in the aging process and is associated with depression, anxiety, and trauma:

"Serum PTH levels were significantly correlated with age, 25OHD and calcium intake..."



6. Vitamin D (cholecalciferol) has been found to suppress PTH at around ~40 ng/ml:

"...There was a strong inverse relationship between 25OHD and PTH."

"...Maximum PTH suppression, does not occur until at least 25OHD levels ≥40 ng/ml."



7. Supplementing with vitamin D (cholecalciferol) does not increase 1,25-D — it lowers it:

"...With high dose vitamin D3 therapy... PTH is physiologically down-regulated and therefore the synthesis of 1,25-D and dietary calcium absorption are reduced."




8. Like vitamin D (cholecalciferol), dietary or supplemental calcium suppresses PTH and 1,25-D:

"Oral calcium supplementation in these men was also accompanied by a reduction in the plasma concentration of PTH and 1,25-D..."


9. Apparently, PTH becomes harder to suppress as a person becomes sicker or older; therefore, every physiological inhibitor (e.g., CO2, calcium, magnesium, vitamin D, vitamin K, etc.) is probably valuable to maintain good health.

 

Inaut

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Here are some more good studies from Danny Roddys telegram :

2.…It is important to point out that low levels of parathyroid hormone (PTH) are essential for maintaining healthy bone structure and normal remodeling."
— Endocrine Physiology by Constance R. Martin

3. PTH and 1,25-D (calctriol or "active" vitamin D) cause hypercalcemia and calcification:

"Severe hypercalcemia is mainly caused by inappropriately high concentrations of compounds which promote bone resorption, in particular PTH, PTHrP, or 1,25-D."



4. The popular "metabolic syndrome,” that involves diabetes, hypertension, and obesity, is associated with higher parathyroid hormone (PTH):

"The PTH level... is an independent predictor of metabolic syndrome..."


5. PTH tends to rise in the aging process and is associated with depression, anxiety, and trauma:

"Serum PTH levels were significantly correlated with age, 25OHD and calcium intake..."



6. Vitamin D (cholecalciferol) has been found to suppress PTH at around ~40 ng/ml:

"...There was a strong inverse relationship between 25OHD and PTH."

"...Maximum PTH suppression, does not occur until at least 25OHD levels ≥40 ng/ml."



7. Supplementing with vitamin D (cholecalciferol) does not increase 1,25-D — it lowers it:

"...With high dose vitamin D3 therapy... PTH is physiologically down-regulated and therefore the synthesis of 1,25-D and dietary calcium absorption are reduced."




8. Like vitamin D (cholecalciferol), dietary or supplemental calcium suppresses PTH and 1,25-D:

"Oral calcium supplementation in these men was also accompanied by a reduction in the plasma concentration of PTH and 1,25-D..."


9. Apparently, PTH becomes harder to suppress as a person becomes sicker or older; therefore, every physiological inhibitor (e.g., CO2, calcium, magnesium, vitamin D, vitamin K, etc.) is probably valuable to maintain good health.

Keep up the good work @Mauritio !!!!!!!!
 
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Mauritio

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"Severe hypercalcemia is mainly caused by inappropriately high concentrations of compounds which promote bone resorption, in particular PTH, PTHrP, or 1,25 (OH)2D3."

 

Recoen

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This Textbook was recommended by ray as a generell overview of endocrinology. There's a lot more but I cant copy it all. I'll upload the book.


TEXTBOOK OF ENDOCRINE PHYSIOLOGY
Constance R. Martin, Ph.D.


REGULATI ON OF PARATHYROID
HORMONE SECRETION
By sharp contrast, very different mechanisms are required for regulation of parathyroid gland function. The parathyroid hormone acts rapidly on kidney and more slowly on bone to elevate calcium ion concentrations of the blood plasma . A very brief period of calcium ion deficiency leads to heightened neuromuscular excitabil ity
which is manifested first in exaggerated reflex responses, but is soon fol lowed in rapid succession by involuntary tremors, muscle spasms, convulsions, and finally release
to renal excret ion of inorganic
Phosphate is increased, with the result that
some of the plasma calcium previously
associated with phosphate becomes available as free calcium ion, as renal loss of calcium may be promptly diminished .
Parathyroid hormone also acts more slowly to
Release calcium from bone reserves, and continued calcium deficiency stimulates parathyroid hormone synthesis . High levels of calcium ion in the circulating blood exert an inhibitory influence on cells of the parathyroid gland.The control mechanism is summarized m Ftgure 2-4. A second hormone, calcitonin (CT, thyrocalcitonin), produced in the thyroid
glands of mammals by cells not involved in
thyroxine secretion ( and in the ultimo-
branchial bodies of other vertebrates) , has
been implicated in protection against an
excessive rise in the calcium ion concentra-
tion of the blood plasma. Its secretion is
triggered by the calcium rise. CT may be
needed under special circumstances (e.g. ,
during absorption of a calcium-rich meal
following a period of fasting) because the
inhibitory influence of calcium ions on the
secretion of parathyroid hormone may not
exert sufficiently rapid influences on blood
concentrations of the ion. CT favors reten-
tion of calcium and phosphate in bone, an
influence which is effectively ( but not directly) antagonistic to the actions of para-
thyroid hormone.
Additional details on regulation of calcium ion concentrations not directly relevant to this discussion are presented in
Section IV.


Parathyroid hormone influences on renal
phosphate and calcium excretion have been
widely studied. But the hormone also promotes
excret ion of sodium, potassium, bicarbonate,
and water, and high doses can induce dehydra-
t ion. Parathyroid hormone also decreases excre-
tion of magnesium and ammonium ions. High
plasma calcium levels which follow administra-
tion of the hormone have been i mplicated in
i nhibition of ADH actions on the renal distal
tubule and collecting ducts.

Lactate Formation and Related Con-
cepts. Other investigators called attention
to the increased rate of glycolysis in bone
after administration of parathyroid hor-
mone, and suggested that lactate ( rather
than citrate) is the agent responsible for
bone decalcification. A further modifica-
tion of the general concept states that it is
the reduction of pH in bone tissue (rather
than the accumulation of a specific anion)
which promotes bone solubilization. Car-
bonic acid has also been proposed to con-
tribute to acidity changes.
Martin’s textbook can be found here:
 
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